Ejersted C, Andreassen T T, Hauge E M, Melsen F, Oxlund H
Department of Connective Tissue Biology, University of Aarhus, Denmark.
Bone. 1995 Dec;17(6):507-11. doi: 10.1016/8756-3282(95)00371-1.
Human parathyroid hormone 1-34 (PTH) exerts an anabolic effect on bone in younger rats. The aim of the present study was to examine the effect of PTH on vertebral bone in 2-year-old male rats. The rats were treated with daily injections of 15 nmol/kg PTH or vehicle (V) for 56 days. Tetracycline and calcein were injected on day 15 and day 40 of the treatment period, respectively. The PTH treatment did not influence the body weights of the rats, the volumes of whole vertebra, or the vertebral body heights. However, the PTH treatment induced profound changes in the bone structure. Histomorphometric analyses of the vertebral bodies (L-6) revealed an approximate doubling of the cancellous bone volume after PTH treatment from 24.6 +/- 1.3% to 54.9 +/- 2.0% (p < 0.001) as well as a doubling of the trabecular thickness while the bone surface/bone volume decreased by 60%. PTH treatment also increased bone formation as indicated by an increase in mineral apposition rate (from 0.42 +/- 0.01 to 0.89 +/- 0.01 microns/day, p < 0.01), increased mineralizing surface (from 7.8 +/- 1.4 to 43.8 +/- 1.9%, p < 0.01) and an increase in both volume-related and surface-related bone formation rates (5 and 11 times, respectively). The biomechanical properties were analyzed using standardized bone specimens from the vertebral bodies of L-4 by applying cranial-caudal compression in a materials testing machine. The PTH treatment induced a substantial increase in the strength of the vertebral body: ultimate load increased by 66%, ultimate stiffness by 47%, and energy absorption by 98%. The increase in vertebral body strength was also evident after normalizing the parameters to the cross sectional area and the ash content of the vertebral body specimens. PTH treatment increased ultimate stress from 26 +/- 3 to 44 +/- 3 N per mm2 (p < 0.01) and increased ultimate load normalized to ash content per mm specimen height from 59 +/- 4 to 72 +/- 4 N (mm/mg) (p < 0.05). The PTH treatment induced an increase in dry defatted bone density and ash density of both the vertebral body specimen (L-4) and the whole vertebra (L-5). In conclusion, PTH showed a remarkable ability to stimulate bone formation in the vertebral body of old rats. Furthermore, the biomechanical analysis revealed an enhanced compressive bone strength, even after correction for the increased bone mass, indicating an improved bone quality after the PTH treatment.
人甲状旁腺激素1 - 34（PTH）对年轻大鼠的骨骼具有合成代谢作用。本研究的目的是检测PTH对2岁雄性大鼠椎骨的影响。大鼠每天注射15 nmol/kg PTH或赋形剂（V），持续56天。在治疗期的第15天和第40天分别注射四环素和钙黄绿素。PTH治疗不影响大鼠体重、整个椎骨体积或椎体高度。然而，PTH治疗引起了骨结构的深刻变化。对椎体（L - 6）的组织形态计量学分析显示，PTH治疗后松质骨体积从24.6±1.3%增加到54.9±2.0%，约增加了一倍（p < 0.001），小梁厚度也增加了一倍，而骨表面/骨体积减少了60%。PTH治疗还增加了骨形成，表现为矿物质沉积率增加（从0.42±0.01增加到0.89±0.01微米/天，p < 0.01）、矿化表面增加（从7.8±1.4增加到forty - three point eight plus or minus one point nine percent，p < 0.01）以及体积相关和表面相关骨形成率均增加（分别增加了5倍和11倍）。使用来自L - 4椎体的标准化骨标本，在材料试验机上施加头 - 尾向压缩来分析生物力学性能。PTH治疗使椎体强度大幅增加：极限载荷增加了66%，极限刚度增加了47%，能量吸收增加了98%。将参数归一化到椎体标本的横截面积和灰分含量后，椎体强度的增加也很明显。PTH治疗使极限应力从26±3增加到44±3 N/mm²（p < 0.01），并使归一化到每毫米标本高度的灰分含量的极限载荷从59±4增加到72±4 N（mm/mg）（p < 0.05）。PTH治疗使椎体标本（L - 4）和整个椎骨（L - 5）的脱脂干骨密度和灰分密度均增加。总之，PTH显示出显著刺激老年大鼠椎体骨形成的能力。此外，生物力学分析表明，即使在校正增加的骨量后，压缩骨强度仍增强，表明PTH治疗后骨质量得到改善。
